PMID- 26063408
OWN - NLM
STAT- MEDLINE
DCOM- 20160802
LR  - 20150929
IS  - 1099-1263 (Electronic)
IS  - 0260-437X (Linking)
VI  - 35
IP  - 11
DP  - 2015 Nov
TI  - Bisphenol A affects placental layers morphology and angiogenesis during early 
      pregnancy phase in mice.
PG  - 1278-91
LID - 10.1002/jat.3176 [doi]
AB  - Bisphenol A (BPA) is a widespread endocrine disrupter mainly used in food contact 
      plastics. Much evidence supports the adverse effects of BPA, particularly on 
      susceptible groups such as pregnant women. The present study considered placental 
      development - relevant for pregnancy outcomes and fetal nutrition/programming - 
      as a potential target of BPA. Pregnant CD-1 mice were administered per os with 
      vehicle, 0.5 (BPA05) or 50 mg kg(-1) (BPA50) body weight day(-1) of BPA, from 
      gestational day (GD) 1 to GD11. At GD12, BPA50 induced significant degeneration 
      and necrosis of giant cells, increased vacuolization in the junctional zone in 
      the absence of glycogen accumulation and reduction of the spongiotrophoblast 
      layer. In addition, BPA05 induced glycogen depletion as well as significant 
      nuclear accumulation of beta-catenin in trophoblasts of labyrinthine and 
      spongiotrophoblast layers, supporting the activation of the Wnt/beta-catenin 
      pathway. Transcriptomic analysis indicated that BPA05 promoted and BPA50 
      inhibited blood vessel development and branching; morphologically, maternal 
      vessels were narrower in BPA05 placentas, whereas embryonic and maternal vessels 
      were irregularly dilated in the labyrinth of BPA50 placentas. Quantitative 
      polymerase chain reaction evidenced an estrogen receptor beta induction by BPA50, 
      which did not correspond to downstream genes activation; indeed, the 
      transcription factor binding sites analysis supported the AhR/Arnt complex as 
      regulator of BPA50-modulated genes. Conversely, Creb appeared as the main 
      transcription factor regulating BPA05-modulated genes. Embryonic structures 
      (head, forelimb) showed divergent perturbations upon BPA05 or BPA50 exposure, 
      potentially related to unbalanced embryonic nutrition and/or to modulation of 
      genes involved in embryo development. Our findings support placenta as an 
      important target of BPA, even at environmentally relevant dose levels.
CI  - Copyright (c) 2015 John Wiley & Sons, Ltd.
FAU - Tait, Sabrina
AU  - Tait S
AD  - Food and Veterinary Toxicology Unit, Department of Veterinary Public Health and 
      Food Safety, Istituto Superiore di Sanita, Rome, Italy.
FAU - Tassinari, Roberta
AU  - Tassinari R
AD  - Food and Veterinary Toxicology Unit, Department of Veterinary Public Health and 
      Food Safety, Istituto Superiore di Sanita, Rome, Italy.
FAU - Maranghi, Francesca
AU  - Maranghi F
AD  - Food and Veterinary Toxicology Unit, Department of Veterinary Public Health and 
      Food Safety, Istituto Superiore di Sanita, Rome, Italy.
FAU - Mantovani, Alberto
AU  - Mantovani A
AD  - Food and Veterinary Toxicology Unit, Department of Veterinary Public Health and 
      Food Safety, Istituto Superiore di Sanita, Rome, Italy.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150609
PL  - England
TA  - J Appl Toxicol
JT  - Journal of applied toxicology : JAT
JID - 8109495
RN  - 0 (Benzhydryl Compounds)
RN  - 0 (CTNNB1 protein, mouse)
RN  - 0 (Endocrine Disruptors)
RN  - 0 (Phenols)
RN  - 0 (beta Catenin)
RN  - MLT3645I99 (bisphenol A)
SB  - IM
MH  - Animals
MH  - Benzhydryl Compounds/*toxicity
MH  - Dose-Response Relationship, Drug
MH  - Endocrine Disruptors/toxicity
MH  - Female
MH  - Gene Expression Profiling
MH  - Mice
MH  - Phenols/*toxicity
MH  - Placenta/*drug effects
MH  - Pregnancy
MH  - Pregnancy Outcome
MH  - Reproducibility of Results
MH  - Trophoblasts/drug effects/metabolism
MH  - Wnt Signaling Pathway
MH  - beta Catenin/metabolism
OTO - NOTNLM
OT  - Bisphenol A
OT  - blood vessels
OT  - developmental toxicity
OT  - endocrine disruption
OT  - toxicogenomics
OT  - trophoblast
EDAT- 2015/06/13 06:00
MHDA- 2016/08/03 06:00
CRDT- 2015/06/12 06:00
PHST- 2015/02/18 00:00 [received]
PHST- 2015/04/10 00:00 [revised]
PHST- 2015/04/19 00:00 [accepted]
PHST- 2015/06/12 06:00 [entrez]
PHST- 2015/06/13 06:00 [pubmed]
PHST- 2016/08/03 06:00 [medline]
AID - 10.1002/jat.3176 [doi]
PST - ppublish
SO  - J Appl Toxicol. 2015 Nov;35(11):1278-91. doi: 10.1002/jat.3176. Epub 2015 Jun 9.